Pyroptosis, a novel mechanism implicated in cataracts.

Abstract

An understanding of the mechanism of cataract formation may reduce its burden on medical care worldwide. It is established that pyroptosis is associated with oxidative stress, one of the causes of cataracts, and may provide novel therapeutic targets for the treatment of cataracts. The present study therefore investigated the role of pyroptosis in cataract formation. SRA01/04 human lens epithelium cells (HLECs) were treated with H2O2 and cell viability was assessed by an MTT assay. Pyroptosis in HLECs was examined by TUNEL staining, and the expression of caspase‑1 and interleukin (IL)‑1β was determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot analysis and immunostaining. A caspase‑1 inhibitor was used to investigate the effects of caspase‑1 downregulation. In addition, the expression of caspase‑1 and IL‑1β in lens anterior capsule tissue samples from patients with cataracts and normal controls was also analyzed by immunostaining, RT‑qPCR and western blot analysis. The results demonstrated that pyroptosis in H2O2‑treated HLECs, and the mRNA and protein expression of caspase‑1 and IL‑1β, was significantly increased compared with control cells. Furthermore, caspase‑1 and IL‑1β expression was significantly increased in cataract tissue samples compared with normal controls. When HLECs were cotreated with a caspase‑1 inhibitor and 100µM H2O2, caspase‑1 and IL‑1β expression were decreased compared with the 100µM H2O2‑only group. In conclusion, the results of the present study demonstrate that pyroptosis may have a role in cataract formation, and the caspase‑1 and IL‑1β pathways may be involved in this pathological process. Pyroptosis appears to be a promising target in the prevention of cataract formation.